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作 者:光红梅[1] 魏欣冰[1] 李应全[1] 仲英[2] 左春旭[2] 张岫美[1]
机构地区:[1]山东大学医学院药理学研究所,济南250012 [2]山东省医学科学院药物研究所,济南250062
出 处:《中国药学杂志》2008年第13期982-986,共5页Chinese Pharmaceutical Journal
基 金:国家自然科学基金(30572187)
摘 要:目的研究过氧化氢损伤牛脑微血管内皮细胞(BCMEC_s)的机制及羟乙葛根素的保护作用。方法比色法测定培养液中乳酸脱氢酶(LDH)活性,硫代巴比妥酸法测定细胞内和培养液中脂质过氧化产物丙二醛(MDA)含量,黄嘌呤氧化酶法检测细胞内和培养液中超氧化物歧化酶(SOD)的活性,放射性免疫法检测细胞培养液中血栓素A_2的最终代谢产物血栓素B_2(TXB_2)的水平和前列环素最终代谢产物6-酮基前列腺素1α(6-keto-PGF1α)的含量。结果H_2O_2(200μmol·L^(-1))损伤后,BCMEC_sLDH释放水平、MDA含量呈时间依赖性增加,SOD活性呈时间依赖性降低,羟乙葛根素能够呈浓度依赖性降低LDH水平和MDA含量,提高SOD活性;H_2O_2(200μmol·L^(-1))损伤BCMEC_s后,细胞培养液中TXB_2含量显著升高、6-keto-PGF1α含量显著降低,羟乙葛根素能够呈浓度依赖性降低TXB_2含量、升高6-keto-PGF1α水平。结论羟乙葛根素对过氧化氢损伤BCMEC_s后的脑血管内皮细胞功能具有保护作用,其机制与抗氧化作用有关。OBJECTIVE To investigate the mechanism of bovine cerebral microvascular endothelial cells ( BCMECs ) damages induced by hydrogen peroxide and evaluate the protective effects of hydroxyethylpuerarin on the injured BCMECs. METHODS Cells injury was determined by lactate dehydrogenase (LDH) activity in the extracellular medium. Malondialdelyde (MDA) and superoxide dismutase(SOD) activity both intracellular and in the extracellular medium were quantified by their reagents and the absorbance was assessed by automatic biochemistry analyser. Radioimmunoassay was applied to measure the amount of thromboxane B2 (TXB2) and 6- keto-prostaglandin F1 α (6-keto-PGF1 α) secreted by BCMECs. RESULTS The exposure of cells to H2O2 ( 200 μmol·L^-1 ) for 2, 4 and 8 h caused a significant increase of LDH leakage, MDA level, and decrease of SOD activity compared with the normal group. Pre-incubation for 24 h with different concentrations of hydroxyethylpuerarin decreased the level of LDH and MDA, and increased the activity of SOD in a concentration-dependent manner in H2O2-induced cells. H2O2 also damaged the cells by increasing the content of TXB2 and decreasing the content of 6-keto-PGF1α secreted by BCMECs. Hydroxyethylpuerarin reduced the content of TXB2 and increased the content of 6-keto-PGF1α in a concentration-dependent manner. CONCLUSION Hydroxyethylpuerarin protects the function of BCMECs against hydrogen peroxide-induced injury contributing to its antioxidant effects.
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